(English) Neuroinflammation and Neurotransmission Mechanisms Involved in Neuropsychiatric Disorders


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Neuroinflammation and Neurotransmission Mechanisms Involved in Neuropsychiatric Disorders
Jacqueline A. Leite*, Ana Maria M. Orellana*, Paula F. Kinoshita*, Natália P. de Mello*, Cristoforo Scavone, Elisa M. Kawamotoδ
Pharmacology Department, Institute of Biomedical Sciences, University of São Paulo, Brazil
Abstract: Some classical psychiatric disorders such as schizophrenia, autism, major depression, bipolar and obsessive-compulsive disorders have been related to neuroinflammatory process, immunological abnormalities and neurotransmission impairment beyond genetic mutations. Neuroinflammation is mostly regulated by glial cells which respond to physiological and pathological stimuli by anti- and pro-inflammatory cytokine and chemokine signaling, moreover recent studies have indicated that glial cells also respond to the neurotransmitters. Neurotransmitters regulate many biological processes, such as cell proliferation and synaptogenesis, which contribute to the formation of functional circuits. Alterations in the neurotransmission can lead to many pathological changes that occur in brain disorders. For example, studies have shown that neuroinflammation can alter the metabolism of glutamate as well the function of its transporters, resulting in cognitive, behavioral, and psychiatric impairments. Cytokines as IL-1β and IL-6 appear to have an important influence in the dopaminergic and serotoninergic neurons. These data together suggest that glial cells via cytokines and abnormal regulation of neurotransmitters can influence psychiatric disorders. The present knowledge about this issue does not allow answering whether neuroinflammation is the cause or the consequence of neurotransmission imbalance and emphasizes the importance to improve in vivo imaging methods and models to elucidate this enigma.
Keywords: Neuroinflammation, neurotransmitters, psychiatric disorders
Book title: Mechanisms of Neuroinflammation – In Tech Open Science